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First of all I would like to thank Nigel for providing a link to a copy of Paul's paper which I have read with interest. I congratulate Paul on doing a nice summary of some of the important MS literature going back 150 years. This is somewhat deja vu for me because C. pneumone as the cause of MS burst on the scene in 1998, only 3 years after I had begun my quest to identify as many causal factors as possible.

Paul references a number of studies which found C. pneumonia in PwMS but failed to list all the studies which did not, and there are lots of them. The most convincing study that C.pneumonia is NOT a key causal factor of MS is the Munger et al, 2004 study which looked at the blood samples of people who later developed MS. It is critical to note that these samples were collectected after the time MS is established (>18) and before MS was diagnosed. To quote the authors, "Seropositivity for Cpn was not significantly associated with risk of MS". This seriously downgrades the C.pneumonia hypothesis because the cause must come before the disease.

I might also note that Paul did not address the genetics of MS and the strong HLA evidence. This also downgrades an infective hypothesis. It should also be noted that immunosuppressants have some, albeit relatively minor, benefit for MS and they should have the opposite effect if MS is primarily an infectious disease as Paul proposes. I would also mention that it appears CCSVI is relatively common (at least 10% of healthy controls) whereas MS is rare (~.1% of population). Thus only one person in 100 with CCSVI gets MS. The bottom line is CCSVI is most important for MS to happen but there are other rarer factors which are also causal factors. The evidence for EBV in MS is extremely strong. A similar Harvard study to the Munger one on C.pneumomia found that everyone who got MS had an EBV infection before diagnosis.

Of course the pediatric studies also leave little doubt that EBV is a key player in MS. I expect CCSVI is caused by a variety of factors perhaps including C.pneumone. To me all the data for MS are best explained by MS being caused by the presence of CCSVI (variety of causes and quite common) in concert with a dysregulated immune system most likely due to genetics (rare), and an EBV infection during vitamin D deficiency (common). Finally I would note the geography of MS is readily explained by vitamin D supply and genetics and in no way points to an infectious cause for MS.

I know the Munger study. It tracked serum IgG in a very large cohort. Cart before the horse, in my opinion. IgG is not that reliable. C. pneumoniae was found readily in the MS brain at Vanderbilt after extensive culturing.

I am not sure regarding the HLA. I would have to look into that. Which studies is he citing?

Also, regarding EBV. I'm not downplaying its significance. Rather, IF EBV was involved. Its role would not be the same as C. pneumoniae. Since Chlamydophila have shown to be pro-artherosclerotic (narrowing, inflammation, etc.). This might be the same process going on in the stenosed veins. I haven't found any lit regarding EBV provoking this kind of response in vivo.

Yet, if I have to venture: I would assume that EBV's process would be mainly auto-immune, and in my opinion, have the OPPOSITE effect to what Embry pointed out: that immunosuppressants WOULD, in fact, work (which they obviously don't, in the long run especially for neurodegeneration, at least for that matter). Of course, one has to remember that C. pneumoniae's initial role is an upper respiratory tract infection (most common at age ~10). Its role changes as the pathogen becomes chronic and becomes less susceptible to the immune response.

Regarding the "commonality" of CCSVI. C. pneumoniae is a fairly ubiquitous organism and much of the population has been exposed to it at some point. This could, in turn, mirror the "commonality" of the CCSVI. However, until a VERY large study has been conducted. I would hold off on making any statements, or believing any, on how common this condition really is.

Then again, I'm not saying any of you are wrong or CCSVI is bs. Just discussing.

I am not sure about your questions (you have very many broad-ranging inquiries). I understand that C. pneumoniae is a very common bacteria that presents itself initially as an upper or lower respiratory tract infection. According to Thibault's review, there are different serovars and I quote:

Chlamydial infections are associated with a range of chronic disease that are characterized by inflammation and scarring and result in significant damage to the host. Chlamydiophila trachomatis serovars A to C cause the ocular infection trachoma which results in blindness. Ascending infection by serovars D to K of the female genital tract causes salpingitis which in turn leads to fibrosis, scarring, stenosis and obstruction of the fallopian tubes with the eventual complications of ectopic pregnancy and tubal infertility.[37]

The Paul le Gac papers that Thibault quotes are located on Wheldon's website. Le Gac also mentions that the bacterial pathogen implicated in a portion of his cases of multiple sclerosis originated from the "Chlamydiacae superfamily."

I am not an authority on this bacteria. There could be different forms or strains which contribute to different pathologies (i.e., one strain will create minimum stenosing or artherosclerosis and instead promote chronic low-grade asthma e.g.,). Let me quote Wheldon, from his website:

An elucidation of the possible events which may happen in the course of persistent infective states with this organism will present one of the greatest challenges in medical microbiology in this century.

Mudhut, Manitoba -- April 1, 2010 -- A study published in the April 1 parchment issue of the journal Milkology shows that smoking banana peel may increase the risk of multiple symbiosis ("MS") in people who also have specific established risk factors for "MS".

The research involved 4 people with "MS" and 8 people without the disease from 3 studies: the Banana-peel Study, the Bottle-fed "MS" Study, and the Epstein-Beatle "MS" Study.

Researchers first determined whether participants had known risk factors for "MS", including having a high level of Auntie Bobbie in the blood to the Epstein-Beatle papyrus virus or having the East-LA gene, which is largely present in patients with MS.

The study found that among those with high levels of Auntie Bobbie to the Epstein-Beetle papyrus virus, banana-peel smokers were twice as likely to have "MS" as those who had never smoked the peel

The same association was not seen in those with low Auntie Bobbie levels.

The risk of "MS" associated with peel smoking was not different in people with and without the East LA gene.

"The consistency of an association between "MS", smoking peels, and Bobbie's immune response to the Epstein-Beatle papyrus virus based on these 3 distinct, pornographically diverse studies suggests this finding is not due to pants," said study author Sting, Tantric School of Pubic Health, New York. "This relationship may provide clues as to why certain individuals develop pictures while others develop "MS"."

In the United States, the average lifetime risk of developing multiple symbiosis is approximately 1 in 200 for women and 1 in 600 for men. Among those with high Auntie Bobby levels to the Epstein-Beatle papyrus virus, peel-smokers may have up to a 2-fold increase in MS risk compared with non-banana-peel-smokers.

It was also found that:

If the Epstein-Beatles Battle Auntie Bobbie's Papyrus Virus in a Bottle, and the Banana-Peel is Smoking with the Tokens in a Tunnel, it's called an

NoDrainer wrote:What would happen if CCSVI patients took the CAP course before the procedure.

Could this be the answer (inflammation anesthetic) for all forms of restenosis, beating it to the punch?

. . . and provide the proof as to why some do not restenose?

I like the concept, I would also like to think there is a test to prove that there is a problem first! And that there are tissue samples taken and tested to give an indication of what the vein walls are like before bombing with products!

Technology may not be there yet? Tissues samples taken by catheter?

Looking forward to answers before treatment, so that there is not a new issue introduced!

MS is multifactorial. That means many factors are involved in the etiology of MS not just vascular and bacterial factors. The same factors are not involved in everyone who develops MS. Please open your minds when thinking about MS etiology. Please understand that we do not understand the etiology of MS.I hope that CCSVI advocates are open minded - CPn is a factor in MS in some people, but not everyone. Treat CPn if the symptoms are present (see Dr David Wheldan's protocol for regime).I am disappointed that Phebologists are engaging in a turf war with Neurologists, with pwMS losing as a result. I hoped that we had moved on since 12 Jul 2010 when London's Daily Telegraph reported, 'Walker believes a “turf war” is under way between neurologists here who believe they “own” MS, and radiologists and vascular surgeons who may have something to contribute to its management. Patients are being caught in the crossfire. ' (http://www.telegraph.co.uk/health/78823 ... elief.html).

The first treatment for pwMS should be high dose Vitamin D3. Then a reveiw of the patient's history should determine the next steps.

MarkW

PS I have been taking David Wheldon's Combined Antibiotic Protocol for CPn many years, and included CPn in my MS studies. Conclusion = CPn is a factor for some pwMS but not everyone.

CureOrBust wrote:I took the CAP for 12 months approximately 5 years before my CCSVI procedure and as far as I know, I have not restonosed. However, neither treatments have alleviated my MS symptoms.

Did you have confirmed virus thought?

Antibiotics are only for Bacteria, not virus.Confirming that I have the bacteria CPn is of no benefit, as everyone basically has it, its the chronic infection of the CNS that is attempted to be treated, and a PCR of your CNS "material" is not really an option for patients.

I welcome your comments Ashton. Yes ther have been just as many negative studies with Cpn as positive, but that is now also true of CCSVI. Do you dismiss CCSVI also because of the now considerable number of negative studies. About 40% of my MS patients are sero-positive for Cpn. Of those that are sero-positive and have gone onto a prolonged (6 month) course of the combined antibiotic protocol, all (only a handful so far) have become sero- negative, which to me indicates that they have had a persisting chronic infection that is now controlled. I have been impressed with the clinical results with RR MS patients having no further relapses and progressives stabilising. Some have had venoplsties as well, some haven't. The serology for Cpn unfortunately is unreliable, and MS patients who have negative serology often still benefit from the CAP.

It is likely that Cpn is therfore not the only agent that may cause this syndrome despite what Kurtzke once said -" (neurologists) are pulling the cart(the immune reaction) before the horse (infective agent), and it is likely to be just one horse rather than a herd". Genetic evidence (which isn't strong in any case) does not downgrade the infective hypothesis as there may be genetic factors which influence the susceptibilty to infection or the likelihood of an infection going on to cause the cascade of problems seen in MS.

Cpn is not showing up in 100%...it's in 40% of Dr. Thibault's MS patients. The serology is unreliable. And Dr. Thibault agrees that Cpn is not the only agent that may cause this syndrome...We need to look at the big picture--and how the endothelium is affected by many factors.Bacteria, viruses, lifestyle, diet, toxins, nutritional deficiencies, etc.cheer

Surely the Lab would be able to tell him the sero-positive % of non MS patients? and I would be more interested in its effects on the MS disease and/or symptoms, rather than some random bacterial infection. All that these number4s appear to prove, are that the antibiotics work. We would already know this I would think.

cheerleader wrote:Cpn is not showing up in 100%...it's in 40% of Dr. Thibault's MS patients. The serology is unreliable. And Dr. Thibault agrees that Cpn is not the only agent that may cause this syndrome...We need to look at the big picture--and how the endothelium is affected by many factors.Bacteria, viruses, lifestyle, diet, toxins, nutritional deficiencies, etc.cheer

My study tells me that we need to look at the big picture of MS, so we agree.However you speak only about "how the endothelium is affected by many factors". The big picture means considering the immune and vascular systems not just one of them. Hence for me the starting point of treatment for MS is Vitamin D3 and Omega 3. I don't have sufficient data to say which will impact which system to the greater extent. But as both supplements are low cost, it must not be a choice and both must be taken before and after de-stenosis.

CPn is an interesting and difficult situation. Is the dormant bacteria causing the vascular endothelium to change or maybe activating a gene and enhancing the immune cascade ??? Frankly, I do not need to know in order to recommend Dr David Wheldon's CAP regime in cases where CPn is probably present in pwMS. Bacterial die off reactions (when starting the CAP) are more reliable than serology in detecting the presence of dormant CPn bacteria.

CureOrBust wrote:Surely the Lab would be able to tell him the sero-positive % of non MS patients? and I would be more interested in its effects on the MS disease and/or symptoms, rather than some random bacterial infection. All that these number4s appear to prove, are that the antibiotics work. We would already know this I would think.

Your faith in labs CureOrBust is higher than mine. Remember the CPn bacteria is dormant and hiding inside cells so serum lab work is rarely conclusive. You may be interested to know that, David Wheldon (Consultant Microbiologist) did not use tests when I consulted him (some years ago).

I stick with the thought "MS is multifactorial". Starting point of treatment for MS is Vitamin D3, Omega 3 and healthy living. Next get a 'gold standard' diagnosis and treatment for CCSVI syndrome (I realise not everyone can afford this). If you are offered immune system drugs (by your health system) please try them, they may work. Consider bacterial treatment, they may work. Viruses (EBV, HHV etc) are too widespread to treat in pwMS.

Please try not to get stuck in a vascular or immune silo..........MS is multifactorial. It is of unknown etiology. Unfortunately we have to live with it.

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